Ferrara Silvia, Falcone Marilena, Macchi Raffaella, Bragonzi Alessandra, Girelli Daniela, Cariani Lisa, Cigana Cristina, Bertoni Giovanni
Department of Biosciences, Università degli Studi di Milano, Milano, Italy.
Infections and Cystic Fibrosis Unit, Division of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Milano, Italy.
PLoS One. 2017 Jun 30;12(6):e0180386. doi: 10.1371/journal.pone.0180386. eCollection 2017.
Small non-coding RNAs (sRNAs) are post-transcriptional regulators of gene expression that have been recognized as key contributors to bacterial virulence and pathogenic mechanisms. In this study, we characterized the sRNA PesA of the opportunistic human pathogen Pseudomonas aeruginosa. We show that PesA, which is transcribed within the pathogenicity island PAPI-1 of P. aeruginosa strain PA14, contributes to P. aeruginosa PA14 virulence. In fact, pesA gene deletion resulted in a less pathogenic strain, showing higher survival of cystic fibrosis human bronchial epithelial cells after infection. Moreover, we show that PesA influences positively the expression of pyocin S3 whose genetic locus comprises two structural genes, pyoS3A and pyoS3I, encoding the killing S3A and the immunity S3I proteins, respectively. Interestingly, the deletion of pesA gene results in increased sensitivity to UV irradiation and to the fluoroquinolone antibiotic ciprofloxacin. The degree of UV sensitivity displayed by the PA14 strain lacking PesA is comparable to that of a strain deleted for pyoS3A-I. These results suggest an involvement of pyocin S3 in DNA damage repair and a regulatory role of PesA on this function.
小非编码RNA（sRNA）是基因表达的转录后调节因子，已被认为是细菌毒力和致病机制的关键因素。在本研究中，我们对机会性人类病原体铜绿假单胞菌的sRNA PesA进行了表征。我们发现，在铜绿假单胞菌PA14菌株的致病岛PAPI-1内转录的PesA有助于铜绿假单胞菌PA14的毒力。事实上，pesA基因缺失导致菌株致病性降低，感染后囊性纤维化人支气管上皮细胞的存活率更高。此外，我们表明PesA对绿脓菌素S3的表达有正向影响，其基因座包含两个结构基因pyoS3A和pyoS3I，分别编码杀伤蛋白S3A和免疫蛋白S3I。有趣的是，pesA基因的缺失导致对紫外线照射和氟喹诺酮抗生素环丙沙星的敏感性增加。缺乏PesA的PA14菌株表现出的紫外线敏感性程度与缺失pyoS3A-I的菌株相当。这些结果表明绿脓菌素S3参与DNA损伤修复，且PesA对该功能具有调节作用。
